Search results for "Nitrovasodilator"

showing 5 items of 5 documents

Reduction of infarct size by the NO donors sodium nitroprusside and spermine/NO after transient focal cerebral ischemia in rats

2000

Nitric oxide (NO) plays a dual role (neuroprotection and neurotoxicity) in cerebral ischemia. NO promoting strategies may be beneficial shortly after ischemia. Therefore, we have studied the hemodynamic and possible neuroprotective effects of two NO donors, the classical nitrovasodilator sodium nitroprusside (SNP) and the NONOate spermine/NO, after transient focal cerebral ischemia in rats. Parietal cortical perfusion was measured by laser-Doppler flowmetry. The effects of increasing intravenous doses (10-300 microgram) of sodium nitroprusside and spermine/NO on cortical perfusion and arterial blood pressure were assessed. Transient (2 h) focal cerebral ischemia was carried out by the intra…

MaleNitroprussideVasodilator AgentsIschemiaSpermineBlood PressurePerfusion scanningBrain damagePharmacologyNitric oxidechemistry.chemical_compoundAnimalsMedicineNitric Oxide DonorsRats WistarMolecular Biologybusiness.industryCerebral infarctionGeneral NeuroscienceBrainCerebral Infarctionmedicine.diseaseRatschemistryIschemic Attack TransientAnesthesiaSpermineNeurology (clinical)Sodium nitroprussidemedicine.symptombusinessNitrovasodilatorDevelopmental Biologymedicine.drugBrain Research
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Nitric oxide is involved in non-adrenergic, non-cholinergic inhibitory neurotransmission in rat duodenum

1995

1. In rat duodenum, electrical field stimulation (EFS) induced a relaxation due to activation of non-adrenergic, non-cholinergic (NANC) inhibitory intramural neurones. 2. Nitric oxide synthase (NOS) inhibitors, N omega-nitro-L-arginine (L-NNA) and N omega-nitro-L-arginine methyl ester (L-NAME), caused a dose-dependent reduction in amplitude of the NANC relaxation. Responses to low frequencies of stimulation were more sensitive to NOS inhibitors than those to high frequencies. 3. Effects induced by NOS inhibitors were stereospecific since D-NNA and D-NAME did not affect NANC relaxation. L-arginine, but not D-arginine, partially prevented the effects induced by NOS inhibitors on NANC relaxati…

MaleNitroprussidemedicine.medical_specialtyDuodenumMuscle RelaxationStimulationIn Vitro TechniquesArginineAutonomic Nervous SystemNitric OxideNitroarginineSynaptic TransmissionNitric oxidechemistry.chemical_compoundNitroarginineInternal medicineMedicineAnimalsChymotrypsinRats WistarPharmacologybiologybusiness.industrymusculoskeletal neural and ocular physiologyGeneral NeuroscienceMuscle SmoothElectric StimulationRatsNitric oxide synthaseMuscle relaxationEndocrinologyNG-Nitroarginine Methyl EsterchemistryTetrodotoxinbiology.proteinSodium nitroprussideAmino Acid OxidoreductasesNitric Oxide SynthasebusinessNitrovasodilatormedicine.drug
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Relaxant effects of sodium nitroprusside and NONOates in goat middle cerebral artery: delayed impairment by global ischemia-reperfusion.

1999

Global cerebral ischemia and subsequent reperfusion induce early impairment of the vasodilator responses to hypercapnia and vasoactive substances. Nitric oxide (NO) is involved in the regulation of cerebral blood flow (CBF) in both health and disease. The present study was designed to assess possible changes in the cerebrovascular reactivity to NO donors induced by cerebral ischemia-reperfusion in goats. Female goats (n = 9) were subjected to 20 min global cerebral ischemia under halothane/N2O anesthesia. Sixteen additional goats were sham-operated as a control group. One week later the effects of ischemia-reperfusion on relaxations to NO donors sodium nitroprusside (SNP), diethylamine/NO (…

NitroprussideCancer ResearchPhysiologyMuscle RelaxationClinical BiochemistryCerebral arteriesIschemiaVasodilationPharmacologyBiochemistrymedicine.arterymedicineAnimalsNitric Oxide Donorsbusiness.industryGoatsCerebral Arteriesmedicine.diseaseCerebral blood flowAnesthesiaReperfusion InjuryMiddle cerebral arteryFemaleSodium nitroprussideHalothanebusinessNitrovasodilatormedicine.drugNitric oxide : biology and chemistry
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The effects of the nitric oxide donors molsidomine and SIN-1 on human polymorphonuclear leucocyte functionin vitro andex vivo

1992

The nitrovasodilator and nitric oxide donor molsidomine and its metabolite SIN-I dilate vascular smooth muscle and inhibit platelet activation by increasing intracellular concentrations of cyclic GMP We have therefore studied the effects of molsidomine and SIN-I on isolated human polymorphonuclear leucocytes (PMN)in vitro andex vivo. In vitro molsidomine dose-dependently reducedβ-glucuronidase release and the generation of superoxide anions from non-activated and from FMLP- or PAF-stimulated human PMNs. SIN-1 was equally effective in reducing (β-glucuronidase release and totally inhibited oxygen radical generation at a concentration of 580 μmol · l−1. In a double-blind, placebo-controlled, …

PharmacologyMolsidomineChemistrySuperoxideMetabolitehemic and immune systemsGeneral MedicinePharmacologyNitric oxidechemistry.chemical_compoundBiochemistryIn vivomedicinePharmacology (medical)Platelet activationNitrovasodilatorEx vivomedicine.drugEuropean Journal of Clinical Pharmacology
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Number of nitrate groups determines reactivity and potency of organic nitrates: a proof of concept study in ALDH-2−/− mice

2007

Background and purpose: Mitochondrial aldehyde dehydrogenase (ALDH-2) has been shown to provide a pathway for bioactivation of organic nitrates and to be prone to desensitization in response to highly potent, but not to less potent, nitrates. We therefore sought to support the hypothesis that bioactivation by ALDH-2 critically depends on the number of nitrate groups within the nitrovasodilator. Experimental approach: Nitrates with one (PEMN), two (PEDN; GDN), three (PETriN; glyceryl trinitrate, GTN) and four (pentaerithrityl tetranitrate, PETN) nitrate groups were investigated. Vasodilatory potency was measured in isometric tension studies using isolated aortic segments of wild type (WT) an…

Pharmacologychemistry.chemical_classificationbiologyAldehyde dehydrogenasePentaerythritol tetranitrateDehydrogenaseNitric oxidechemistry.chemical_compoundEnzymeBiochemistrychemistrymedicinebiology.proteinStructure–activity relationshipPotencyNitrovasodilatormedicine.drugBritish Journal of Pharmacology
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